(Circulation. 2001;103:2428.)
© 2001 American Heart Association, Inc.
Special Report |
Coronary Heart Disease in the First 30 Years of the 21st Century: Challenges and Opportunities
The 33rd Annual James B. Herrick Lecture of the Council on Clinical Cardiology of the American Heart Association
Presented at the Annual Meeting of the American Heart Association’s Council on Clinical Cardiology, New Orleans, La, November 14, 2000.
From the Cardiovascular Division, Department of Internal Medicine, University of Virginia Health System, Charlottesville, Va.
Key Words: coronary disease • diabetes mellitus • myocardial infarction • obesity
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Introduction |
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During the past 50 years, there has been an explosion of new knowledge regarding the biological mechanisms of cardiovascular disease. This knowledge and the emergence of new technology and new pharmacological, interventional, and surgical therapies, coupled with lifestyle changes in the American population, have contributed to a spectacular 60% decline in mortality from coronary heart disease (CHD) and stroke.1 Since 1965, there has been a dramatic and steady decline in CHD deaths. This marked decrease in the mortality rate for CHD can be attributed in part to enhanced survival in patients with an acute myocardial infarction (MI); highly effective secondary prevention measures in patients who have experienced an ischemic event; improved lifestyles in the population, with some progress in primary prevention of CHD; and advances in medical therapy and the emergence of coronary revascularization. With respect to the decline in CHD mortality from 1980 to 1990, 25% can be explained by primary prevention, 29% by secondary prevention, and 72% by the improvements in medical therapy and revascularization; only 3% is unexplained.2
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Improved Prognosis After Acute MI |
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Figure 1
depicts a significant decrease in the death rate
and case fatality rate for acute MI among persons 45 to 64 years of age
in the United States from 1970 through
1995.3 In Osler’s
Textbook of Medicine published
in 1892,4 only 2 pages were
dedicated to a discussion of acute MI. This foremost educator of his
era wrote, "A complete obliteration of one coronary artery,
if produced suddenly, is usually
fatal."4 It was James B.
Herrick (born in 1861) who changed our perception regarding this dire
prognosis for patients with acute MI. In his historical article
published in the Journal of the American
Medical Association in 1912,5 Herrick
stated:
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"One may conclude, therefore, from a consideration of the clinical histories of numerous cases ... , from animal experiments, and from anatomic study that there is no inherent reason why this stoppage of a large branch of a coronary artery or even of a main trunk must of necessity cause sudden death. Rather, it may be concluded that while sudden death often does occur, yet at times it is postponed for several hours or even days, and in some instances, a complete, that is functionally complete, recovery ensues."
If James B. Herrick were alive today, he would be amazed at how often such a "functionally complete" recovery actually does ensue: it is now the norm rather than the exception.
Prognosis after recovery from MI continues to improve, and much of the progress in recent years can be attributed to postinfarction therapeutic interventions. At the annual meeting of the European Society of Cardiology in Amsterdam in August 2000, Wallentin6 provided data regarding the effectiveness of 2 of these interventions, early statin therapy and coronary angioplasty, in >22 000 patients with acute MI from the Swedish National Registry of Cardiac Intensive Care. His group found that starting statins in the hospital after MI reduced 1-year mortality by 34%. Early coronary revascularization reduced mortality by 36%. The combination of starting statins in the hospital and coronary angioplasty reduced mortality by a remarkable 64%. Another recent study showed a 25% reduction in 1-year mortality when statins were started in the hospital for acute MI patients.7
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Improving Survival After Acute MI |
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We can still do better to improve survival after acute MI. More expansive and effective out-of-hospital defibrillation for potential sudden death victims and preventing delays to initial reperfusion therapy must be accomplished. More effective (ie, TIMI 3 flow) and earlier opening of an occluded infarct vessel and more potent adjunctive therapies in the acute phase of MI to salvage jeopardized myocardium and to prevent infarct vessel reocclusion need to be developed. Some have advocated out-of-hospital fibrinolysis only when a physician is present or out-of-hospital time is
60
minutes.8 In the future,
out-of-hospital pharmacological reperfusion and antithrombotic therapy
may become more feasible to administer in most patients with acute MI.
Pharmacological therapy other than angiotensin-converting
enzyme (ACE) inhibitors and ß-blockers that is aimed at
attenuating left ventricular remodeling and preventing
congestive heart failure must be introduced. In the future, myogenesis
therapy to repopulate myocytes in areas of damaged
myocardium will certainly be forthcoming. Preliminary data
from Dr R. Chiu’s laboratory at McGill University suggest that adult
stem cells from the bone marrow injected into the damaged hearts of
rats can differentiate into viable heart muscle
cells.9 For patients with
severely damaged myocardium, xenotransplantation with
hearts from cloned pigs may become feasible. Better mechanical hearts
than those previously tested could emerge as long-term alternatives to
heart transplantation or more tolerable bridges to transplantation.
Noninvasive imaging technologies performed in conjunction with exercise
or pharmacological stress to identify high-risk postinfarction patients
who may benefit from invasive strategies are being perfected. Also,
additional secondary prevention measures to retard or reverse the
underlying atherosclerotic process and to prevent the rupture of
vulnerable plaques to enhance long-term survival are currently under
investigation.
Reduction of prehospital deaths must be accomplished to make
further major inroads with respect to reducing mortality in patients
with acute MI.10 Such deaths
comprise >50% of the deaths of patients with acute MI who die in the
first 30 days.11 Prevention
of the "no reflow" phenomenon from occurring after reperfusion
using better adjunctive therapy is another goal for clinical
researchers in the field of acute MI research. Angiographic no reflow,
which is defined as TIMI 2 flow or less, predicts long-term mortality
after acute infarction.12 No
reflow is associated with subsequent left ventricular
remodeling, heart failure, and premature death. Measures to improve
outcome with reperfusion are continually being reported
(Figure 2).13 As
shown in a recent study,13
the cumulative incidence of death, reinfarction, or stroke was reduced
by 34% in patients who received a glycoprotein IIb/IIIa
platelet antagonist and underwent coronary
stenting compared with those who received thrombolytic
therapy with tissue plasminogen activator
alone. In the group that received a coronary stent plus
abciximab, the median size of the final infarct was 14.3% of the left
ventricle, as compared with a median of 19.4% in the
thrombolytic therapy alone group. Other pharmacological
adjunctive therapies such as adenosine
infusion14 are undergoing
clinical trials at the present time.
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Although the proportion of acute MI patients developing heart failure during hospitalization has declined substantially since 1975, the 1-year discharge mortality rate for MI survivors with congestive heart failure has not changed in the 20-year period between 1975 and 1995, even after controlling for additional prognostic characteristics.15 The authors of the study that reported this data concluded that long-term prognosis did not improve over this 20-year period because MI survivors with heart failure in the 1990s are increasingly older and have more comorbidities than postinfarction patients who developed heart failure in the 1970s.15 The 1-year follow-up of the Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries (GUSTO)-III study16 showed that the 1-year mortality rate in patients who received thrombolytic therapy had increased compared with the mortality rate of patients followed-up in the GUSTO-I trial. They found it "disturbing" that, in light of the more intensive pharmacological interventional after MI with aspirin, statins, ß-blockers, and ACE-inhibitors, a 35% increase in late deaths was observed compared with the mortality reported in the 1996 GUSTO-I trial. These data highlight the need for substantially improved postinfarction treatment strategies in the upcoming years to diminish the incidence of heart failure and late cardiac deaths in the MI population that is becoming more elderly and represents a higher-risk group because of significant comorbidities.
Some elderly patients with acute MI are not benefiting from the advances in therapy already implemented in everyday clinical practice. Berger et al17 found that less than half of elderly patients considered ideal candidates for reperfusion therapy received primary angioplasty or thrombolysis within 6 hours of hospital arrival.17 Similarly, the percentage of eligible elderly patients receiving ACE inhibitors for heart failure is suboptimal.18 Thus, not only must we continue to make new discoveries that improve the survival and quality of life for MI patients, but we also need to implement proven diagnostic and therapeutic strategies better in this patient population.
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An Increasing Elderly Population |
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Heart failure from several causes and chronic CHD will be encountered with greater frequency as our population ages. In 1900, only 4% of the population reached 65 years of age. By 2010,
35% of
the population will be older than 65 years of age. By 2025, 62 million
people in the United States will be 65 years or older. By 2050, the
number of Americans 65 years of age or older is estimated to rise to
78.8 million
(Figure 3).19 This
increased longevity will contribute to the increased incidence of
cardiovascular disease and the increased number of
deaths from heart disease and stroke. According to the American Heart
Association’s statistical update for
2000,20 59 700 000
Americans had cardiovascular disease. Of these,
12 200 000 had CHD, 7 200 000 have had a MI, and 4 600 000 were
alive with congestive heart failure. Heart failure is now the most
common diagnosis in hospitalized patients 65 years of age or older.
This is not surprising because the incidence of heart failure increases
substantially with advancing age, particularly in
men.21
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As would be expected, the older an individual is when he or she develops heart failure, the worse the prognosis. As age increased from <55 years to >84 years in the survey by MacIntyre et al,22 the 1-year case fatality rate for patients with heart failure increased from 24.2% to 58.1%. In this retrospective analysis, mortality averaged 44.5% in the 66 547 patients with heart failure (mean age, 75 years).22 Thus, one of the main challenges for cardiovascular specialists over the next 30 years will be to prevent heart failure from occurring in our increasingly elderly population. However, when it occurs, effective therapeutic measures to reduce mortality and to enhance quality of life need to be promptly instituted.23 One effective means of reducing the incidence of heart failure in the elderly is better treatment systolic hypertension, one of the major contributing pathogenic factors for heart failure (as well as stroke) in this population.24
The elderly will also contribute to an increased prevalence of CHD in the first 30 years of the new millennium. From 2000 to 2030, as the baby boomers continue to augment the ranks of seniors, the prevalence of CHD will increase by >50%.19 As suggested, a growing elderly population will be the main driving force for this increase in CHD.
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Epidemic of Type 2 Diabetes |
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Increasing Prevalence of Type 2 Diabetes
In addition to the increase in the elderly population, the epidemic of type 2 diabetes will lead to a striking increase in the number of young individuals with CHD in the United States and worldwide. This is because diabetes increases the risk of CHD 2- to 4-fold. Presently, 10.2 million Americans have diabetes; it is estimated that 5.4 million have undiagnosed diabetes.25 Two-thirds of these patients will die of heart or blood vessel disease. The risk of diabetes for Mexican-Americans and non-Hispanic blacks is twice that for non-Hispanic whites.20 For people in their 40s, the incidence of diabetes increased 40% from 1990 to 1998. For people in their 30s, it rose nearly 70%.26 In 1999 alone, the incidence of diabetes rose an astounding 6% compared with the previous year.27 By 2025, the number of adults with diabetes will rise to 300 million worldwide compared with 135 million 5 years ago.28 Diabetes is estimated to increase by 42% in developed countries, but a 170% increase is expected in developing countries, with India and China showing the greatest increase.28 Today, children as young as 8 years old are being diagnosed with type 2 diabetes.29 As noted by Dr Richard Kahn, type 2 diabetes was virtually unheard of in children just a decade ago, and now as many as 300 000 children have it.29 A consensus panel of the American Academy of Pediatrics and American Diabetes Association issued recommendations concerning the prevalence of diabetes among children.30 The panel noted that type 2 diabetes is an "emerging epidemic" among children. This disorder used to be called "adult-onset diabetes" because of its tendency to emerge in middle age or later. Because of its increased prevalence in children and young adults, it is now simply called "type 2 diabetes" to distinguish it from juvenile diabetes, which is now known as "type 1 diabetes."
Diabetes and Cardiovascular
Outcomes
Diabetes adversely affects
cardiovascular outcomes. Diabetics with no clinical
evidence of CHD have the same risk for future cardiac death as
nondiabetics with a prior
infarction.31 The absolute
risk of CHD death at any concentration of cholesterol is 3
to 5 times higher in the presence of
diabetes.32 Diabetes
increases the risk of cardiac events and mortality in patients with
established CHD. The cardiovascular mortality rate has
more than doubled in men and more than quadrupled in women who have
diabetes compared with
nondiabetics.32 33
Diabetics have increased mortality and morbidity after
thrombolysis for an acute
MI,34 and they have a worse
prognosis with unstable angina and a worse outcome after
percutaneous coronary intervention.
Figure 431 shows
the MI rate in nondiabetics with or without a prior infarction compared
with the rate in diabetics with or without a prior infarction. Note
that diabetics with or without a prior infarction have a markedly
higher risk of a new infarction than do nondiabetics. What is
impressive is the observation that 45% of diabetics with a previous
infarction will experience a recurrent infarction.
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The 2-year prognosis of diabetics who are hospitalized with unstable angina or non-Q-wave MI is significantly worse than nondiabetics.35 From the prospectively collected data from 6 different countries participating in the Organization to Assess Strategies for Ischemic Syndromes (OASIS) registry, diabetes independently predicted mortality (relative risk, 1.57), cardiovascular death, new MI, stroke, and new congestive heart failure. Diabetic patients with no previous cardiovascular disease had the same long-term morbidity and mortality as did nondiabetic patients with established cardiovascular disease after hospitalization for an acute coronary syndrome.35
Diabetics do worse with primary angioplasty than do
nondiabetics.36 In one
survey, the mortality rate after primary angioplasty, both in-hospital
and at 1 year, was 2-fold higher for diabetics than for the entire
group of patients evaluated
(Figure 5). Diabetics in the Bypass Angioplasty
Revascularization Investigation (BARI) registry who
underwent multivessel coronary angioplasty had a significantly
higher all-cause mortality and cardiac mortality at 5 years after
revascularization than did patients who were
randomized to coronary bypass
surgery.37 Cardiac mortality
was 23% for diabetics undergoing angioplasty compared with 8% for
those undergoing bypass surgery. Recent data have shown that
glycoprotein IIb/IIIa platelet receptor
antagonists can improve outcomes and reduce subsequent
ischemic cardiac events in diabetic patients undergoing
percutaneous coronary
intervention.38
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Great efforts are being made to reduce cardiovascular morbidity and mortality in diabetics with improved medical therapy, and studies like those reported from the Heart Outcomes Prevention Evaluation (HOPE) trial are encouraging.39 In this trial, cardiovascular death was reduced by 37% and total mortality by 24% in diabetics randomized to ramipril therapy compared with placebo. Lowering LDL cholesterol with hydroxymethylglutaryl coenzyme A reductase inhibitors (statins) in diabetics with preexisting CHD yields a significant benefit with respect to reduction of subsequent CHD events.40
Pathophysiology of Type 2 Diabetes and
CHD
Certain concepts have emerged regarding how the
pathophysiology of type 2 diabetes leads to
cardiovascular
disease.41
Saltiel42 outlines the
metabolic staging of type 2 diabetes, providing a basis for
understanding the mechanism by which this disorder promotes
atherosclerosis. As shown in
Figure 6, type 2 diabetes begins with peripheral
insulin resistance contributed to mainly by obesity.
Hyperinsulinemia, a consequence of this insulin
resistance, can be detected long before impaired glucose tolerance
occurs. Insulin resistance is a common state and is also associated
with aging, a sedentary lifestyle, and a genetic
predisposition.43 Impaired
insulin action and hyperinsulinemia lead to a
variety of other abnormalities, including elevated
triglycerides, low levels of HDL cholesterol,
enhanced secretion of VLDL, disorders of coagulation, increased
vascular resistance, central obesity, hypertension, and
atherosclerosis. Eventually, pancreatic ß-cells can
no longer compensate for the insulin-resistant state. This
leads to decreased insulin secretion and glucose intolerance. Finally,
full-blown ß-cell failure and loss of insulin secretion occur,
yielding the late diabetes syndrome.
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Atherosclerosis may develop in young adults who have the early diabetic state of insulin resistance before an increased fasting blood glucose level is detected. McGill et al44 quantified the extent of atherosclerosis in the aorta and right coronary artery of persons aged 15 to 34 years who died of external causes. An association between atherosclerotic lesions and elevated glycohemoglobin levels obtained from postmortem blood was observed. The thickness of the panniculus adiposus and body mass index were associated with more extensive fatty streaks in the right coronary artery and aorta. These data and data from other similar studies are indeed disturbing. Because hyperinsulinemia can occur a decade before an elevation of fasting blood glucose, the atherosclerotic process may be well underway before such patients come to the attention of a physician.
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The Obesity Epidemic |
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Epidemiology of Obesity
As depicted in Figure 6
, obesity is the major driving force in the
development of type 2 diabetes. In the United States, the age-adjusted
prevalence of obesity increased by 30% from 1980 to
1994.45 Obesity is estimated
to account for 325 000 deaths annually in the United
States.46 Overweight means
having a body mass index 25
kg/m2.47
Obesity is defined as having a body mass index 30
kg/m2 (30 pounds overweight). Obesity
increased from a prevalence of 14.5% in the US population during the
period of 1976 to 1980 to 22.5% from 1994 to
1998.48
Table 1 shows the marked increase in the prevalence
of obesity and weight in US adults from 1991 to
1998.49 In 1998, 54% of
Americans were considered overweight, and 23% were considered obese,
with 1 in 10 children being
obese.50 From 1963 to 1990,
there was a 42% increase in the prevalence of obesity in children.
Over a period of 14 years from 1980 to 1994, the prevalence of obesity
in children doubled from 6.5% to 11.4% in children aged 6 to 11
years.51
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Of great importance is that 60% of overweight children 5 to
10 years of age already have one associated biochemical or clinical
cardiovascular risk factor, such as
hyperlipidemia, hypertension, or
hyperinsulinemia, and 25% have 2 risk factors
that are observed to lead to CHD in
adults.52 According to
Koplan and Dietz,47 almost
80% of obese adults have diabetes, high blood cholesterol
levels, high blood pressure, coronary artery disease,
gallbladder disease, or osteoarthritis, and almost 40% have 2 of
these comorbidities. These figures are indeed frightening, because
obesity is associated with an almost 3-fold higher risk of
cardiovascular disease mortality and a 2-fold risk of
all-cause
mortality.53
Causes of Increased Obesity
The causes of obesity are related to genetic factors,
physical activity, and poor nutrition. The latter is particularly
characterized by the increased ingestion of "fast foods" in this
country, which are high in both fat and total calories. Genetic factors
can be magnified by lifestyle changes with respect to the propensity
for developing type 2 diabetes. Japanese Americans have a higher
prevalence of type 2 diabetes than do people in
Japan.54 This has been shown
to be a consequence of the development of central obesity due to a diet
higher in animal fat and decreased physical activity, leading to
insulin resistance in the Japanese living in the United
States.55 This occurs in the
face of a genetic background of reduced ß-cell reserve in all
Japanese.55
In addition to poor nutrition and genetic factors, physical
inactivity plays a major part in the increased incidence of obesity and
type 2 diabetes. In the United States, 50% of youth aged 12 to 21
years are not vigorously active on a regular
basis.56 Twenty-five percent
of Americans are sedentary, and only 15% of US adults engage in
regular physical activity, which is defined as exercising 3 times a
week for at least 20
minutes.56 Inactivity by
itself is a risk factor that increases CHD
risk.57 The benefits of
physical activity and exercise are shown in
Table 2.58
Benefits include diminished cardiovascular mortality
and development of CHD, a lowered blood pressure in hypertensive
patients, an increase in insulin sensitivity, prevention of obesity, an
elevation of HDL cholesterol, a favorable effect on the
fibrinolytic system, enhanced endothelial function, and
enhanced parasympathetic activity.
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As caregivers, cardiologists have a professional obligation
to promote increased, regular physical activity in the population. The
importance of physician counseling cannot be
overemphasized.59 It is as
important as counseling for better nutrition. Data suggest that only
one third of patients are counseled by physicians regarding beginning
or continuing an exercise
program.59 Merely counseling
obese women to engage in a program of reducing caloric intake to
1200 kcal/day, to eat a low-fat diet, and to incorporate increased
lifestyle activity resulted in health benefits (ie, weight loss and
lowering of cholesterol and triglycerides)
comparable to a program of diet and regular aerobic exercise
sessions.60
We must teach our medical students, medical residents, and cardiology fellows to convey to patients the importance of physical activity as a means to prevent or reduce obesity, type 2 diabetes, and prevalence of CHD. Parents have an obligation to teach children that physical activity is part of normal life, and schools have a responsibility to start offering physical education to students again. Schools are not doing a very good job when it comes to physical fitness. The New York Times reported that 1 in 4 children gets no physical education in school and that Illinois is the only state that requires daily physical education for all children.61 High school students’ enrollment in daily physical education classes plummeted from 42% in 1991 to 25% in 1995.56
Our children are taking in excess energy over energy
expenditure, leading to the storage of that excess in the form of fat.
Decreased energy expenditure is due to a more sedentary lifestyle
characterized by watching more television and playing more computer
games. The average child in the 6- to 11-year age range watches
25 hours of television per
week.61 Boys and girls who
watched 4 hours of television each day had greater body fat and a
greater body mass index than did those who watched <2 hours per
day.62 Just a 5% to 10%
loss of body weight can improve glucose tolerance,
hyperlipidemia, and hypertension in obese children and
adults.63 According to the
Surgeon General’s Report on Physical
Activity and Health, just a moderate amount of physical
activity (eg, 30 minutes of brisk walking or raking leaves, 15 minutes
of running, or 45 minutes of playing volleyball) on most, if not all,
days of the week is all that is necessary to obtain significant health
benefits.56
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Impact on Increasing Prevalence of CHD on Costs of Health Care |
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The increasing prevalence of cardiovascular disease being fueled by the epidemics of obesity and type 2 diabetes and the aging of our population will greatly impact the costs of health care. The US healthcare system is the most expensive in the world, with 14% of gross domestic product going to health care in 1998. Expenditures for health care in 1998 totaled
$1 trillion. The estimated cost of
cardiovascular disease and stroke in 2000 was $326.6
billion
(Figure 7).20 As
to cost projections for the future, Steinwachs et
al64 predict that healthcare
costs will increase 41% by 2010 and 54% by 2025. The major driving
force for these increased costs will be the growth in the aging of the
population. Certainly, costs will rise as a function of the increased
prevalence of new cases of CHD contributed to by physical inactivity,
obesity, and type 2 diabetes. Contributing to these rising costs will
certainly be expensive new technology and new pharmaceuticals for the
evaluation and management of the populations of patients with CHD and
heart failure.
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The Future |
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The next 30 years presents us with formidable challenges in the continuing battle to reduce the case fatality rate for CHD, the overall prevalence of CHD, and the prevalence of congestive heart failure in the population. Further advances in basic science research and breakthroughs in clinical care for patients with or at risk for CHD will surely emerge. This progress will have enormous impact in reducing death and morbidity from CHD and preventing its occurrence in the first place. A greater emphasis will need to be placed on the primary prevention of CHD, including educating the public on the need to adhere to a heart-healthy diet, incorporating regular physical activity as part of daily life, and preventing the initiation of smoking in our youth. We must ensure that the quality of cardiovascular care becomes more uniform throughout the United States. The issue of whether more cardiologists should be trained in our fellowship programs to enter the workforce must be addressed. We may not be training a sufficient number of cardiology fellows to meet the needs of the expected increased number of patients with cardiovascular disease. Only 6 years ago, we thought we were training too many cardiology fellows. As the knowledge base in cardiovascular disease continues to grow exponentially, new approaches to disseminating scientific and medical information must be undertaken using innovative electronic online learning technology.
In conclusion, certain predictions can be made with respect to the future.
- Despite a
decrease in mortality rate, the prevalence of CHD and congestive heart
failure will increase, as will the costs of health
care.
- An increasing elderly population and the
epidemic of type 2 diabetes fueled by physical inactivity and obesity
will contribute to the increasing prevalence of CHD in the next 30
years.
- New technology will be introduced that
will be accurate for the preclinical or subclinical detection of
coronary atherosclerosis and vulnerable
plaques. This will have an impact on the further reduction in
coronary events in patients who have
atherosclerosis, with or without
diabetes.
- Genetic screening for future risks of
diabetes and CHD as an outgrowth of the Human Genome Project and
earlier primary prevention measures will hopefully emerge to identify
and treat those at high risk for premature CHD.
- Novel therapeutic interventions for
chronic CHD, such as therapeutic angiogenesis and myogenesis (cell
therapy), will be introduced that will further decrease mortality and
morbidity from CHD for those patients in whom we cannot prevent the
ravages of atherosclerosis.
- Gene therapy, organogenesis for
developing living tissue products, artificial mechanical hearts,
xenotransplantation using pig hearts, and products emanating from
the new field of nanotechnology will become part of our therapeutic
armamentarium.
Although future research and development will bring us new medical discoveries based on progress in technology, we must not forget that less costly, low-tech interventions have already proven effective in preventing CHD and its complications.
I would like to end with a quote from Dr Claude Lenfant’s editorial, "Conquering Cardiovascular Disease: Progress and Promise":65 "Although the potential for the fields of molecular biology and genetics to improve identification of persons and populations at risk, to predict the evolution of a disease in a specific patient, and to optimize pharmacological intervention is exciting and worthy of pursuit, physicians must not lose sight of perhaps more mundane but clearly effective approaches such as lowering blood pressure, reducing obesity and physical inactivity, and applying other proven therapeutic strategies (eg, ß-blockers, aspirin) in a timely fashion. The real challenge of the new millennium may indeed be to strike an appropriate balance between the pursuit of exciting new knowledge and the full application of strategies that are already known to be extremely effective, but are considerably underused."
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Acknowledgments |
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I am grateful for the superb editorial assistance provided by Jerry Curtis in preparing this manuscript.
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Footnotes |
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Reprint requests to Dr Beller, Cardiovascular Division, Department of Medicine, University of Virginia Health System, PO Box 800158, Charlottesville, VA 22908-0158.
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References |
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1. Lewis RP. The ACC at 50: a giant grew in Bethesda: the impact of the ACC on cardiovascular medicine. J Am Coll Cardiol. 2000;35(5 suppl B):60B–65B.
2.
Hunink MG, Goldman L, Tosteson AN, et al. The recent decline in mortality from coronary heart disease, 1980–1990: the effect of secular
trends in risk factors and treatment. JAMA. 1997;277:535–542.
3.
Levy D, Thom TJ. Death rates from coronary disease: progress and a puzzling paradox. N Engl J Med. 1998;339:915–917.
4. Osler W. The Principles and Practice of Medicine. 8th ed. New York: D. Appleton; 1916.
5. Herrick JB. Clinical features of sudden obstruction of coronary arteries. JAMA. 1912;59:2015–2020.
6. Wallentin LC. COHORT registry: Swedish national register of cardiac intensive care with 18,461 patients reporting on the influence of statin therapy at discharge and performance of early revascularisation procedures on one-year mortality. Paper presented at: 22nd Annual Congress of the European Society of Cardiology; August 25–30, 2000; Amsterdam, the Netherlands.
7.
Stenestrand U,
Wallentin L. Early statin treatment following acute myocardial
infarction and 1-year survival: the Swedish Register of Cardiac
Intensive Care (RIKS-HIA).JAMA. 2001;285:430–436.
8. ECC guidelines. Part 7, the era of reperfusion: section 1, acute coronary syndromes (acute myocardial infarction). Circulation. 2000;102(suppl I):I-172–I-203.
9. Wang J-S, Shum-Tim D, Chedrawy E, et al. Marrow stromal cells for cellular cardiomyoplasty: the importance of microenvironment for milieu dependent differentiation. Circulation. 2000;102:II-683. Abstract.
10.
Robertson RM.
Sudden death from cardiac arrest: improving the odds.
N Engl J Med. 2000;343:1259–1260.
11.
Kleiman NS, White
HD, Ohman EM, et al. Mortality within 24 hours of
thrombolysis for myocardial infarction: the importance
of early reperfusion: the GUSTO Investigators (Global Utilization of
Streptokinase and Tissue Plasminogen Activator
for Occluded Coronary Arteries).
Circulation. 1994;90:2658–2665.
12. Morishima I, Sone T, Okumura K, et al. Angiographic no-reflow phenomenon as a predictor of adverse long-term outcome in patients treated with percutaneous transluminal coronary angioplasty for first acute myocardial infarction. J Am Coll Cardiol. 2000;16:1202–1209.
13.
Schömig A,
Kastrati A, Dirschinger J, et al. Coronary stenting plus
platelet glycoprotein IIb/IIIa blockade compared with
tissue plasminogen activator in acute
myocardial infarction: Stent versus Thrombolysis for
Occluded Coronary Arteries in Patients with Acute Myocardial
Infarction Study Investigators. N
Engl J Med. 2000;343:385–391.
14.
Mahaffey KW, Puma
JA, Barbagelata NA, et al. Adenosine as an adjunct to
thrombolytic therapy for acute myocardial infarction:
results of a multicenter, randomized, placebo-controlled trial: the
Acute Myocardial Infarction Study of Adenosine (AMISTAD) Trial.
J Am Coll Cardiol. 1999;34:1711–1720.
15.
Spencer FA, Meyer
TE, Goldberg RJ, et al. Twenty year trends (1975–1995) in the
incidence, in-hospital and long-term death rates associated with heart
failure complicating acute myocardial infarction: a community-wide
perspective. J Am Coll
Cardiol. 1999;34:1378–1387.
16.
Topol EJ, Ohman
EM, Armstrong PW, et al, for the GUSTO-III Investigators. Survival
outcomes 1 year after reperfusion therapy with either alteplase or
reteplase for acute myocardial infarction: results from the Global
Utilization of Streptokinase and t-PA for Occluded Coronary
Arteries (GUSTO) III Trial.
Circulation. 2000;102:1761–1765.
17.
Berger AK,
Schulman KA, Gersh BJ, et al. Primary coronary angioplasty vs
thrombolysis for the management of acute myocardial
infarction in elderly patients.
JAMA. 1999;282:341–348.
18.
The Large State
Peer Review Organization Consortium. Heart failure treatment with
angiotensin-converting enzyme inhibitors in
hospitalized Medicare patients in 10 large states.
Arch Intern Med. 1997;157:1103–1108.
19.
Foot DK, Lewis
RP, Pearson TA, et al. Demographics and cardiology,
1950–2050. J Am Coll
Cardiol. 2000;35:1067–1081.
20. American Heart Association. Heart and Stroke Statistical Update 2000. Dallas, Tex: American Heart Association; 1999.
21.
Zannad F,
Briancon S, Juilliere Y, et al, for the EPICAL Investigators.
Incidence, clinical and etiologic features, and outcomes of advanced
chronic heart failure: the EPICAL study (Epidémiologie de
l’Insuffisance Cardiaque Avancée en Lorraine).
J Am Coll Cardiol. 1999;33:734–742.
22.
MacIntyre K,
Capewell S, Stewart S, et al. Evidence of improving prognosis in heart
failure: trends in case fatality in 66 547 patients hospitalized
between 1986 and 1995.
Circulation. 2000;102:1126–1131.
23.
Konstam MA.
Progress in heart failure management? Lessons from the real
world. Circulation. 2000;102:1076–1078.
24.
Kaplan NM. New
issues in the treatment of isolated systolic hypertension.
Circulation. 2000;102:1079–1081.
25. Diabetes Statistics. Bethesda, Md: National Diabetes Information Clearinghouse, National Institute of Diabetes and Digestive and Kidney Diseases; 1999. NIH publication 99–3926.
26. Kluger J. The diabetes explosion. Time Magazine. September 4, 2000. Available at: http://www.time.com.
27. Diabetes rates rise another 6 percent in 1999 [press release]. Centers for Disease Control and Prevention, January 24, 2001. Available at: http://www.cdc.gov/diabetes/news/docs/010126.htm. Accessed January 26, 2001.
28. King H, Aubert RE, Herman WH. Global burden of diabetes, 1995–2025. Diabetes Care. 1998;21:1414–1431.[Abstract]
29. Schrof J. The silent killer. U S News and World Report. April 12, 1999. Available at: http://www.usnews.com/usnews/issue/990412/nycu/12diab.htm.
30. Elias. M. Tests urged to fight diabetes’ surge in obese kids. U S A Today. February 22, 2000. Available at: http://www.usatoday.com.
31.
Haffner SM, Lehto
S, Rönnemaa T, et al. Mortality from coronary heart disease
in subjects with type 2 diabetes and in nondiabetic subjects with and
without prior myocardial infarction.
N Engl J Med. 1998;339:229–234.
32. Stamler J, Vacarro O, Neaton JD, et al. Diabetes, other risk factors, and 12-yr cardiovascular mortality for men screened in the Multiple Risk Factor Intervention Trial. Diabetes Care. 1993;16:434–444.[Abstract]
33. Kannel WB. Lipids, diabetes, and coronary heart disease: insights from the Framingham Study. Am Heart J. 1985;110:1100–1107.[Medline] [Order article via Infotrieve]
34.
Mak K-H, Topol
EJ. Emerging concepts in the management of acute myocardial
infarction in patients with diabetes mellitus.
J Am Coll Cardiol. 2000;35:563–568.
35.
Malmberg K, Yusuf
S, Gerstein HC, et al, for the OASIS Registry Investigators. Impact of
diabetes on long-term prognosis in patients with unstable angina and
non–Q-wave myocardial infarction: Results of the OASIS (Organization
to Assess Strategies for Ischemic Syndromes) Registry.
Circulation. 2000;102:1014–1019.
36.
Hannan EL, Racz
MJ, Arani DT, et al. Short- and long-term mortality for patients
undergoing primary angioplasty for acute myocardial infarction.
J Am Coll Cardiol. 2000;36:1194–1201.
37.
Detre KM, Guo P,
Holubkov R, et al. Coronary
revascularization in diabetic patients: a
comparison of the randomized and observational components of the Bypass
Angioplasty Revascularization Investigation (BARI).
Circulation. 1999;99:633–640.
38.
Hammoud T,
Tanguay J-F, Bourassa MG. Management of coronary artery
disease: therapeutic options in patients with diabetes.
J Am Coll Cardiol. 2000;36:355–365.
39. Heart Outcomes Prevention Evaluation Study Investigators. Effects of ramipril on cardiovascular and microvascular outcomes in people with diabetes mellitus: results of the HOPE study and MICRO-HOPE substudy. Lancet. 2000;355:253–259.[Medline] [Order article via Infotrieve]
40. Scandinavian Simvistatin Survival Study Group. Randomized trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Simvistatin Survival Study. Lancet. 1994;344:1383–1389.[Medline] [Order article via Infotrieve]
41. DeFronzo RA, Ferrannini E. Insulin resistance: a multifaceted syndrome responsible for NIDDM, obesity, hypertension, dyslipidemia and atherosclerotic cardiovascular disease. Diabetes Care. 1991;14:173–194.[Abstract]
42. Saltiel AR. Series introduction: the molecular and physiological basis of insulin resistance: emerging implications for metabolic and cardiovascular diseases. J Clin Invest. 2000;106:163–164.[Medline] [Order article via Infotrieve]
43. Horikawa Y, Oda N, Cox NJ, et al. Genetic variation in the gene encoding calpain-10 is associated with type 2 diabetes mellitus. Nat Genet. 2000;26:163–175.[Medline] [Order article via Infotrieve]
44.
McGill HC Jr,
McMahan CA, Malcom GT, et al. Relation of glycohemoglobin and adiposity
to atherosclerosis in youth: Pathobiological
Determinants of Atherosclerosis in Youth (PDAY)
research group. Arterioscler Thromb Vasc
Biol. 1995;15:431–440.
45.
Kuczmarski RJ,
Flegal KM, Campbell SM, et al. Increasing prevalence of overweight
among US adults: the National Health and Nutrition Examination Surveys,
1960 to 1991. JAMA. 1994;272:205–211.
46.
Allison DB,
Fontaine KR, Manson JE, et al. Annual deaths attributable to obesity in
the United States. JAMA. 1999;282:1530–1538.
47.
Koplan JP, Dietz
WH. Caloric imbalance and public health policy.
JAMA. 1999;282:1579–1581.
48. Flegal KM, Carroll MD, Kuczmarski RJ, et al. Overweight and obesity in the United States: prevalence and trends, 1960–1994. Int J Obes Relat Metab Disord. 1998;22:39–47.[Medline] [Order article via Infotrieve]
49.
Mokdad AH,
Serdula AH, Dietz WH, et al. The spread of the obesity epidemic in the
United States, 1991–1998.
JAMA. 1999;282:1519–1522.
50. Marquis C. Americans need better diet, new health study reports. New York Times. May 28, 2000. Available at: http://www.nytimes.com.
51. Kolata G. While children grow fatter, experts search for solutions. New York Times. October 19, 2000:A1, A20.
52.
Freedman DS,
Dietz WH, Srinivasan SR, et al. The relation of overweight to
cardiovascular disease risk factors among children and
adolescents: the Bogalusa Heart Study.
Pediatrics. 1999;103:1175–1182.
53.
Wei M, Kampert
JB, Barlow CE, et al. Relationship between low cardiorespiratory
fitness and mortality in normal weight, overweight, and obese men.
JAMA. 1999;282:1547–1553.
54. Fujimoto WY, Bergstrom RW, Boyko EJ, et al. Diabetes and diabetes risk factors in second- and third-generation Japanese Americans in Seattle, Washington. Diabetes Res Clin Pract. 1994;24:S43–S52.
55. Fujimoto WY, Bergstrom RW, Boyko EJ, et al. Type 2 diabetes and the metabolic syndrome in Japanese Americans. Diabetes Res Clin Pract. 2000;50:S73–S76.
56. US Department of Health and Human Services. Physical Activity and Health: A Report of the Surgeon General. Atlanta, Ga: US Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion; 1996.
57.
Blair SN, Kohl HW
3rd, Barlow CE, et al. Changes in physical fitness and all-cause
mortality: a prospective study of healthy and unhealthy men.
JAMA. 1995;273:1093–1098.
58.
Shephar RJ,
Balady GJ. Exercise as cardiovascular therapy.
Circulation. 1999;99:963–972.
59.
Wee CC, McCarthy
EP, Davis RB, et al. Physician counseling about exercise.
JAMA. 1999;282:1583–1588.
60.
Andersen RE,
Wadden TA, Bartlett SJ, et al. Effects of lifestyle activity vs
structured aerobic exercise in obese women: a randomized trial.
JAMA. 1999;281:335–340.
61. Brody JE. Fitness gap is America’s recipe for fat youth. New York Times. September 19, 2000. Available at: http://www.nytimes.com.
62.
Andersen RE,
Crespo CJ, Bartlett SJ, et al. Relationship of physical activity and
television watching with body weight and level of fatness among
children: results from the Third National Health and Nutrition
Examination Survey. JAMA. 1998;279:938–942.
63.
Willett WC, Dietz
WH, Colditz GA. Primary care: guidelines for healthy weight.
N Engl J Med. 1999;341:427–434.
64.
Steinwachs DM,
Collins-Nakai R, et al. The future of cardiology:
utilization and costs of care. J Am
Coll Cardiol. 2000;35:1092–1099.
65.
Lenfant C.
Conquering cardiovascular disease: progress and
promise. JAMA. 1999;282:2068–2070.
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